ArticleCancer research2020
The Tumor Suppressor BAP1 Regulates the Hippo Pathway in Pancreatic Ductal Adenocarcinoma.
Article in Cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Research progress on the regulation of mesothelioma driven by deubiquitinating enzyme BAP1.Clinical and experimental medicine · 2026Review
- CDK6/4 inactivates BAP1 deubiquitinase destabilizing VHL to promote metastatic colonization in liver.Molecular cancer · 2026Article
- The MST4-14-3-3ζ complex promotes pancreatic cancer by activating YAP.Biology direct · 2026Article
- Review
- AMPK-activated BAP1 regulates pVHL stability and tumor-suppressive functions.Cell death and differentiation · 2026Article
- Tumor suppressor BAP1 emerges as a key regulator of metabolism and cell death in tumors.Frontiers in cell and developmental biology · 2026Review
- Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025Review
- The multifaceted roles of deubiquitinating enzymes (DUBs) in pancreatic ductal adenocarcinoma.Cell death & disease · 2025Review
- Molecular Insights into Pleural Mesothelioma: Unveiling Pathogenic Mechanisms and Therapeutic Opportunities.Diagnostics (Basel, Switzerland) · 2025Review
- BAP1 Represses Sequential Activation of IRAKs and NF-κB Signaling in Pancreatic Cancer.International journal of biological sciences · 2025Article
- TRACERx analysis identifies a role for FAT1 in regulating chromosomal instability and whole-genome doubling via Hippo signalling.Nature cell biology · 2025Article
- Circ_0087851 suppresses colorectal cancer malignant progression through triggering miR-593-3p/BAP1-mediated ferroptosis.Journal of cancer research and clinical oncology · 2024Article
- Deubiquitination complex platform: A plausible mechanism for regulating the substrate specificity of deubiquitinating enzymes.Acta pharmaceutica Sinica. B · 2023Review
- YAP/TAZ activation predicts clinical outcomes in mesothelioma and is conserved in in vitro model of driver mutations.Clinical and translational medicine · 2023Article
- Ubiquitin signaling in pancreatic ductal adenocarcinoma.Frontiers in molecular biosciences · 2023Review
- BAP1 in cancer: epigenetic stability and genome integrity.Discover oncology · 2022Review
- YAP1 is essential for malignant mesothelioma tumor maintenance.BMC cancer · 2022Article
- Review
- Monosomy 3 Is Linked to Resistance to MEK Inhibitors in Uveal Melanoma.International journal of molecular sciences · 2021Article
- An Update on the Role of Ubiquitination in Melanoma Development and Therapies.Journal of clinical medicine · 2021Review
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Authors and funding
18 authors at 7 institutions in 4 countries.
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Abstract
The deubiquitinating enzyme BAP1 is mutated in a hereditary cancer syndrome with a high risk for mesothelioma and melanocytic tumors. Here, we show that pancreatic intraepithelial neoplasia driven by oncogenic mutant KrasG12D progressed to pancreatic adenocarcinoma in the absence of BAP1. The Hippo pathway was deregulated in BAP1-deficient pancreatic tumors, with the tumor suppressor LATS exhibiting enhanced ubiquitin-dependent proteasomal degradation. Therefore, BAP1 may limit tumor progression by stabilizing LATS and thereby promoting activity of the Hippo tumor suppressor pathway. SIGNIFICANCE: BAP1 is mutated in a broad spectrum of tumors. Pancreatic Bap1 deficiency causes acinar atrophy but combines with oncogenic Ras to produce pancreatic tumors. BAP1-deficient tumors exhibit deregulation of the Hippo pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.